Icariin protects against sodium azide—induced neurotoxicity by activating the PI3K/Akt/GSK-3β signaling pathway

PeerJ

article

Ying Zhang¹  Nanqu Huang³  Hao Lu¹  Juan Huang¹  Hai Jin⁵  Jingshan Shi¹  Feng Jin¹ 

[1] Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University;Department of Pharmacy, People’s Hospital of Zhongmu;National Drug Clinical Trial Institution, The Third Affiliated Hospital of Zunyi Medical University ,(The First People’s Hospital of Zunyi);School of Public Health, Zunyi Medical University;Institute of Digestive Diseases of Affiliated Hospital, Zunyi Medical University

关键词: Neurodegenerative diseases;    Alzheimer’s disease;    Icariin;    Sodium azide;    Phosphoinositide 3-kinase;    Protein kinase B;    Glycogen synthase kinase-3β;   

DOI  :  10.7717/peerj.8955

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Background Icariin (ICA) is one of the major active flavonoids extracted from the traditional Chinese herb Epimedium brevicornum Maxim and has been shown to have neuroprotective effects. This study was designed to investigate the effect of ICA on sodium azide (NaN3)-induced rat adrenal pheochromocytoma (PC12) cell damage and to further examine the underlying mechanisms. Methods To explore its possible mechanism, we used NaN3 (50 mM)-induced neuronal PC12 cell damage. Cell viability was evaluated by CCK-8 and lactate dehydrogenase (LDH) assays. Mitochondrial membrane potential (MMP) was detected by JC-1. Glucose concentration was assessed by the glucose oxidase method. The role of ICA in the PI3K/Akt/GSK-3β signaling pathway was explored by Western blotting. Results The results indicate that pretreatment with ICA reduced NaN3-induced cell damage and significantly reduced the leakage rate of LDH in PC12 cells. ICA pretreatment increased the MMP and a decrease in glucose concentration indicate increased glucose consumption. Furthermore, the protein levels of p-PI3K (p85), PI3K-110α, p-Ser473-Akt and p-Ser9-GSK-3β were markedly decreased in PC12 cells after NaN3 treatment for 24 h, whereas these effects were reverted after pretreatment with ICA. Tau phosphorylation at the Ser396/404 and Thr217 sites was significantly decreased by pretreatment with ICA. Conclusions These results suggest that ICA protects against NaN3-induced neurotoxicity in PC12 cells by activating the PI3K/Akt/GSK-3β signaling pathway.

【 授权许可】

CC BY